Related Experiment Videos
Persistent HIV-1-specific cellular responses despite prolonged therapeutic viral suppression
Victor Appay1, Pokrath Hansasuta, Julian Sutton
1Medical Research Council Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK. vappay@gwmail.jr2.ox.ac.uk
AIDS (London, England)
|January 25, 2002
Summary
Despite successful antiretroviral therapy (ART), some HIV patients show ongoing viral replication and specific immune responses. This study found immature CD8 T-cells (cytotoxic T lymphocytes) in these individuals, even with suppressed viremia.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Antiretroviral therapy (ART) is the primary treatment for chronic persistent HIV-1 infection, effectively reducing plasma viremia.
- ART can lead to diminished or absent HIV-specific CD8 T-cell responses, a key component of cellular immunity against the virus.
Purpose of the Study:
- To investigate HIV-1 replication and immune responses in patients on long-term ART.
- To characterize the phenotype of HIV-specific CD8 T-cells in patients with persistent viral transcription despite effective treatment.
Main Methods:
- Detection of ongoing HIV-1 replication, including Nef mRNA transcription, in patients receiving ART.
- Quantification of HIV-specific CD8 and CD4 T-cell responses.
- Phenotypic analysis of HIV-specific CD8 T-cells, including perforin levels and CD27 expression.
Main Results:
- Ongoing HIV-1 replication, particularly Nef mRNA transcription, was detected in some patients despite prolonged ART.
- Significant HIV-specific CD8 and CD4 T-cell responses were observed, with strongest responses targeting Nef epitopes.
- HIV-specific CD8 T-cells exhibited low perforin levels and persistent CD27 expression, indicating an immature cytotoxic T-lymphocyte (CTL) phenotype.
Conclusions:
- The persistence of an immature CTL phenotype is unexpected in patients with prolonged viral suppression on ART and concurrent HIV-specific CD4 T-cell activity.
- This finding suggests a complex interplay between viral persistence, ART, and T-cell maturation in chronic HIV infection.